Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. After administration of a new vasopressin analogue (DDAVP), a marked and prolonged antidiuresis occurred in 10 patients with pituitary diabetes insipidus. 2. The antidiuretic effects of single intravenous doses of 0.04--24 mug DDAVP and single intranasal doses of 5--320 mug DDAVP were investigated. Time curves of the antidiuretic responses expressed in changes of urine osmolality (Uosm) and free water clearance per 100 ml GFR (CH2O X 100/GFR) are described. 3. Maximal "peak" response was obtained after an intravenous dose of 1 mug within the first 12 hrs (Uosm was 7--800 mOsm/KgH2O). Further increase of dosage resulted only in prolongation of duration of action (up to 48 hrs) and peak ("plateau") effect (up to 24 hrs). 4. There was a linear relationship between the log dose and log osmolality of urine collected in the second 12 hours after administration of single intravenous and intranasal doses of DDAVP. 5. Comparison of the effects of 1 mug lysine-vasopressin and 1 mug DDAVP revealed only slight differences in peak effects, but extreme differences in duration of action. 6. It is concluded that in the evaluation of a synthetic vasopressin analogue the maximal antidiuretic ability and the prolongation of action have to be analysed separately.
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PMID:The antidiuretic action of 1-deamino-8-D-arginine vasopressin (DDAVP) in man. 95 Feb 63

A definite relationship was found between the dose of DDAVP (1-24 mug intravenously and 5-320 mug intranasally) and the antidiuretic effects (expressed in changes in free water clearance per 100 ml GFR and in urine osmolality determined in 24 hour urine collection periods) in 7 patients with diabetes insipidus. The relationship was more conspicuous when the second 12 hour antidiuretic responses were considered, indicating a dose-dependent prolongation of the antidiuretic action. Time-curves of the antidiuretic responses proved the dose-dependent prolongation of the duration of antidiuretic action. Second 12 hour antidiuretic response increased more markedly when DDAVP was given divided in two doses a day as compared to the effects of the same quantity of the drug given as a single dose; only by the administration of excessive single doses the effects of the divided doses could be reproduced.
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PMID:Relationship between the dose of 1-deamino-8-d-arginine vasopressin (ddavp) and the antidiuretic response in man. 123 81

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP]. 408 72

Experiments were performed with young two-humped camels exposed to 36-hour starvation with free access to water. The renal functions were measured by the standard clearance method. In spite of the administration of 20 micrograms DDAVP, a higher urine flow rate was recorded in the camels subjected to control measurements (feed intake) than in the fasting period (1.45 +/- 0.06 vs. 0.96 +/- 0.06 ml . min-1, P less than less than 0.001). On the second day of fasting the camels had a significantly reduced glomerular filtration rate (GFR 317.5 +/- 23.2 vs. 170.2 +/- 17.4 ml . min-1, P less than 0.001), urea output (700.5 +/- 62.9 vs. 352.2 +/- 64.7 mumol . min-1, P less than 0.005), and fractional excretion of urea (26.9 +/- 2.8 vs. 17.9 +/- 1.7%, P less than 0.01), whereas their tubular resorption. of urea (Reab urea/GFR) increased (6.28 +/- 0.61 vs. 9.12 +/- 0.82 mumol . ml-1, P less than 0.02). No significant difference was found in the concentration of urea in plasma in the fed camels and in fasting camels (8.55 +/- 0.64 vs. 11.18 +/- 1.09 mmol . l-1, N. S.). The creatinine inulin clearance ratio (C creat/Cin) was 0.92 +/- 0.07 when the animals were fed and 1.17 +/- 0.05 when the animals starved (P less than 0.001); this suggests that the clearance of endogenous creatinine is not suitable for GFR measurement in camels under different conditions of nutrition. The kidneys of camels regulate the excretion of urea during short-time fasting mainly through the reduction of glomerular filtration rate and just partly through an increased tubular resorption.
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PMID:[Renal regulation of the excretion of urea in fasting camels]. 643 69

Oral anticoagulants are commonly prescribed in patients with kidney diseases having atrial fibrillation and thromboembolic risk. It is very important to understand their clinical pharmacology and changes that may occur as GFR declines. Risks and benefits of newer oral anticoagulants are different in patients with CKD and patients with ESRD. Patients with GFR < 30 ml/min per 1.73 m2, including those on dialysis, were systematically excluded from landmark trials. All of the NOACs are dependent on renal clearance to some degree and so the risk of NOAC associated bleeding may be expected to be greater in patients with renal failure. Apixaban may be at least as safe as (or possibly safer than) warfarin in individuals with ESRD. Until more data become available, use of dabigatran, rivaroxaban, and edoxaban in patients with CKD stage 5 and ESRD is not indicated. Available strategies for reversing the anticoagulant effect of NOAC are - specific reversal agents available for dabigatran (idarucizumab) and for the oral direct factor Xa inhibitors - andexanet alfa, antifibrinolytic agents, DDAVP and prothrombin complex concentrates (PCCs). In this review clinical and pharmacological aspects of newer oral anticoagulants in the setting of chronic kidney disease will be discussed.
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PMID:Newer Oral Anticoagulant in Chronic Kidney Disease: What we Should Know. 3179 71